In general, PRAs are characterized by initial loss of
rod photoreceptor function followed by that of the cones and for this reason night blindness is the first significant clinical sign for most dogs affected with PRA.
Subretinal injections of adeno - associated virus vectors expressing RPE65 resulted in restoration of
rod photoreceptor function and improved visual function, first in dogs [61, 62] and subsequently in humans [63 — 65].
Not exact matches
B:
Rod and cone
photoreceptors function under the dim and normal light condition, respectively.
A subsequent electroretinography study identified an initial reduction of the cone
photoreceptor function which led to the condition being re-classified as a cone -
rod dystrophy (CRD), rather than a
rod - led PRA, and the disease was termed CORD1 for cone -
rod degeneration 1 [36].
Intriguingly, an identical homozygous mutation was identified in a human patient with recessive retinitis pigmentosa, the human equivalent of PRA, and established the novel retinal gene, PRCD, as an important gene for the maintenance of
rod photoreceptor structure and
function across species.
Evaluation of retinal
function in 15 Swedish vallhund dogs (nine dogs at Stage 2, two dogs at Stage 3, and four normal control dogs) by electroretinography revealed a decrease of both
rod and cone
photoreceptor - mediated
function in Stages 2 and 3 (Fig. 3).
Electroretinography revealed a gradual loss of both
rod and cone
photoreceptor - mediated
function in Stages 2 and 3 of the disease.